Faculty

Ying Huang Professor

Our group investigates mechanisms involved in the post-transcriptional regulation of mitochondrial gene expressions in fission yeast. We have characterized the mitochondrial tRNA 3-end processing enzyme tRNase Z and Ppr10, which acts as a mitochondrial translational activator. Deletion of either tRNase Z or ppr10 causes apoptotic cell death. Deletion of ppr10 appears to increase the cellular iron concentration and induces oxidative stress. These results indicate a link between mitochondrial dysfunction and iron accumulation, which can cause oxidative stress via the Fenton reaction. Interestingly, it has been suggest that mitochondrial dysfunction, iron accumulation and oxidative stress are linked to Parkinson’s disease (PD). Deletion of ppr10 also cause non-sexual flocculation. We also found that Ppr10 interacts with Mpa1. Our ongoing interests include whether genes involved in flocculation and genes involved in iron homeostasis are co-regulated, how cells sense mitochondrial dysfunction, signal transduction cascades associated with oxidative stress, and how Ppr10 activates mitochondrial translation. We are also interested in the nature of interaction between Ppr10 and Mpa1.